CELL-PROLIFERATION AND APOPTOSIS DURING DEVELOPMENT AND AGING OF THE RABBIT CORPUS-LUTEUM

Citation
Sv. Nicosia et al., CELL-PROLIFERATION AND APOPTOSIS DURING DEVELOPMENT AND AGING OF THE RABBIT CORPUS-LUTEUM, Annals of clinical and laboratory science, 25(2), 1995, pp. 143-157
Citations number
39
Categorie Soggetti
Medical Laboratory Technology
ISSN journal
00917370
Volume
25
Issue
2
Year of publication
1995
Pages
143 - 157
Database
ISI
SICI code
0091-7370(1995)25:2<143:CAADDA>2.0.ZU;2-F
Abstract
Corpora lutea (CL) are endocrine ovarian structures that regulate fund amental reproductive events in mammals. The functional lifespan of the se structures is finite as CL regress and cease secreting progesterone after species-dependent intervals during nonfertile postovulatory cyc les or pregnancy. The signals that regulate CL aging are poorly unders tood. This study investigates cell growth and programmed cell death or apoptosis in corpora lutea of New Zealand White rabbits. To study cel l growth, CL were obtained at various postovulatory days (POD) from an imals injected with the deoxyribonucleic acid (DNA) precursor analog b romodeoxyuridine (BUdR). The BUdR-labeled cells were identified by avi din-biotin-complex immunocytochemistry, and the mean proliferation ind ex area computed by image analysis. Apoptotic cells were scored and fu rther identified by in situ demonstration of DNA fragmentation. Prolif eration in parenchymal, stromal, and endothelial CL cells was signific antly elevated at POD 3, 5, 18, and 21 and highest at POD 3 (P < 0.001 ). The number of apoptotic cells was elevated (P < 0.001) at POD 18 an d 21, while 1 percent or less of CL cells were apoptotic at POD 3, 5, and 12. Apoptosis was accompanied by shrinkage or vacuolization of CL cells and increased mean number (P < 0.001) of heterophilic leucocytes at POD 18. These data demonstrate that cell growth is more intense du ring early luteal development and that cell deletion via apoptosis pla ys an important role in CL regression. The role of paracrine signals s uch as microphagic cytokines in CL aging remains to be elucidated.